Effect of Resveratrol on Gliotransmitter Levels and p38 Activities in Cultured Astrocytes

Zhou, Hao; Chen, Qing; Kong, Dan; Guo, Jun; Wang, Qian; Yu, Shou yi

doi:10.1007/s11064-010-0254-8

Cited by 14 publications

(8 citation statements)

References 34 publications

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“…The present data show that the PI3K signaling pathway is involved in the guanosine modulation of the glutamate uptake, which agrees with other studies that demonstrate the ability of guanosine to promote neuroprotection by activation of this pathway [85,90,107]. The MAPK signaling pathway has also been described as a modulator of glutamate uptake [70,71], and guanosine also modulates this pathway [85]. Here, guanosine reversed the decrease in glutamate uptake caused by glucose deprivation; however, this effect was abolished by the p38 MAPK and ERK specific inhibitors.…”

Section: Discussionsupporting

confidence: 93%

“…3d) inhibitors lost the ability to prevent the decreased glutamate uptake activity caused by glucose deprivation. The MAPK signaling pathway has also been described as a modulator of glutamate uptake [70,71]. Because guanosine modulates this pathway [14], we investigated whether the protective effect of guanosine on glutamate uptake was also dependent of p38 MAPK and ERK.…”

Section: Resultsmentioning

confidence: 98%

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Gliopreventive effects of guanosine against glucose deprivation in vitro

Quincozes‐Santos

Bobermin

Souza

et al. 2013

Purinergic Signalling

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Guanosine, a guanine-based purine, is recognized as an extracellular signaling molecule that is released from astrocytes and confers neuroprotective effects in several in vivo and in vitro studies. Astrocytes regulate glucose metabolism, glutamate transport, and defense mechanism against oxidative stress. C6 astroglial cells are widely used as an astrocyte-like cell line to study the astrocytic function and signaling pathways. Our previous studies showed that guanosine modulates the glutamate uptake activity, thus avoiding glutamatergic excitotoxicity and protecting neural cells. The goal of this study was to determine the gliopreventive effects of guanosine against glucose deprivation in vitro in cultured C6 cells. Glucose deprivation induced cytotoxicity, an increase in reactive oxygen and nitrogen species (ROS/RNS) levels and lipid peroxidation as well as affected the metabolism of glutamate, which may impair important astrocytic functions. Guanosine prevented glucose deprivation-induced toxicity in C6 cells by modulating oxidative and nitrosative stress and glial responses, such as the glutamate uptake, the glutamine synthetase activity, and the glutathione levels. Glucose deprivation decreased the level of EAAC1, the main glutamate transporter present in C6 cells. Guanosine also prevented this effect, most likely through PKC, PI3K, p38 MAPK, and ERK signaling pathways. Taken together, these results show that guanosine may represent an important mechanism for protection of glial cells against glucose deprivation. Additionally, this study contributes to a more thorough understanding of the glial-and redox-related protective properties of guanosine in astroglial cells.

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Section: Discussionsupporting

confidence: 93%

Section: Resultsmentioning

confidence: 98%

Gliopreventive effects of guanosine against glucose deprivation in vitro

Quincozes‐Santos

Bobermin

Souza

et al. 2013

Purinergic Signalling

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“…Second, we studied the activation of MAPK signaling pathway which includes three principal subgroups of proteins, extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal kinases (JNKs), and p38 [65–68], which are known to be responsive to stretch-induced injury and to be involved in myelin protein expression. We focused particularly on the effect of stretch on p38 (43 kDa) and ERK1/2 (44 and 42 kDa) in cerebellar slices (Fig.…”

Section: Resultsmentioning

confidence: 99%

Mechanical Stretch of High Magnitude Provokes Axonal Injury, Elongation of Paranodal Junctions, and Signaling Alterations in Oligodendrocytes

et al. 2018

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Increasing findings suggest that demyelination may play an important role in the pathophysiology of brain injury, but the exact mechanisms underlying such damage are not well known. Mechanical tensile strain of brain tissue occurs during traumatic brain injury. Several studies have investigated the cellular and molecular events following a static tensile strain of physiological magnitude on individual cells such as oligodendrocytes. However, the pathobiological impact of high-magnitude mechanical strain on oligodendrocytes and myelinated fibers remains under investigated. In this study, we reported that an applied mechanical tensile strain of 30% on mouse organotypic culture of cerebellar slices induced axonal injury and elongation of paranodal junctions, two hallmarks of brain trauma. It was also able to activate MAPK-ERK1/2 signaling, a stretch-induced responsive pathway. The same tensile strain applied to mouse oligodendrocytes in primary culture induced a profound damage to cell morphology, partial cell loss, and a decrease of myelin protein expression. The lower tensile strain of 20% also caused cell loss and the remaining oligodendrocytes appeared retracted with decreased myelin protein expression. Finally, high-magnitude tensile strain applied to 158N oligodendroglial cells altered myelin protein expression, dampened MAPK-ERK1/2 and MAPK-p38 signaling, and enhanced the production of reactive oxygen species. The latter was accompanied by increased protein oxidation and an alteration of anti-oxidant defense that was strain magnitude-dependent. In conclusion, mechanical stretch of high magnitude provokes axonal injury with significant alterations in oligodendrocyte biology that could initiate demyelination. Electronic supplementary material The online version of this article (10.1007/s12035-018-1372-6) contains supplementary material, which is available to authorized users.

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“…Res inhibits the increase of extracellular Glu levels induced by stretch injuries by enhancing the Glu transporter, thus increasing Glu uptake, glutathione content, glutamine synthetase activity and S 100B (a neurotrophic cytokine) secretion in cortical astrocyte cultures and C6 glioma cells [14,18,19]. Moreover, Res could directly inhibit Glu release in rat cerebrocortical nerve terminals by decreasing mitogen-activated protein kinase activation and, subsequently suppressing voltage-dependent Ca2+ channel activity [20].…”

Section: Res-mediated Neuroprotective Effects Against Glu-induced Excmentioning

confidence: 99%

“…Res has been shown to reduce p 38 mitogenactivated protein kinase (MAPK) activation in cultured astrocytes following a stretch injury; the AMPA receptor is involved in p 38 MAPK activation following an injury [18]. Res also markedly reduced the amplitude and frequency of AMPA-mediated spontaneous excitatory postsynaptic currents in rat hippocampal pyramidal neurons [27].…”

Section: Res-mediated Neuroprotective Effect Against Glu-induced Excimentioning

confidence: 99%

Neuroprotective Effect of Resveratrol Against Glutamate-Induced Excitotoxicity

Zhang¹,

Hao²,

Wang³

et al. 2015

Adv Clin Exp Med

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As the major neurotransmitter in the mammalian central nervous system (CNS), excessive extracellular glutamate (Glu) can activate the Glu receptors and neuronal calcium (Ca2+) overload, then produce neurotoxicity, which is a common pathway for neuronal injury or death, and is associated with acute and chronic neurodegenerative diseases. Therefore, it has been a therapeutic strategy to investigate neuroprotective effects against Glu-induced neurotoxicity for treating both acute and chronic forms of neurodegeneration. Resveratrol (Res), as a naturally occurring polyphenol mainly found in grapes and red wine, has shown a neuroprotective effect in a variety of experimental models for neurodegenerative diseases in vitro and in vivo. This review will focus on the neuroprotective effect of Res against Glu-induced excitotoxicity in neurodegenerative diseases by blocking different Glu receptors and Ca2+ ion channels (Adv Clin Exp Med 2015, 24, 1, 161-165).

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Effect of Resveratrol on Gliotransmitter Levels and p38 Activities in Cultured Astrocytes

Cited by 14 publications

References 34 publications

Gliopreventive effects of guanosine against glucose deprivation in vitro

Gliopreventive effects of guanosine against glucose deprivation in vitro

Mechanical Stretch of High Magnitude Provokes Axonal Injury, Elongation of Paranodal Junctions, and Signaling Alterations in Oligodendrocytes

Neuroprotective Effect of Resveratrol Against Glutamate-Induced Excitotoxicity

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